Differential sensitivity of chronic high-fat-diet-induced obesity in Sprague-Dawley rats

2018 ◽  
Vol 29 (5) ◽  
pp. 553-563 ◽  
Author(s):  
Shakthi R.K. Devan ◽  
Surendar Arumugam ◽  
Ganesh Shankar ◽  
Suresh Poosala
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Differential Sensitivity ◽  
Sprague Dawley ◽  
High Fat ◽  
Diet Induced Obesity ◽  
High Fat Diets ◽  
Fat Diets

AbstractBackgroundThe prevalence of obesity is reported to be increasing owing to the high intake of dietary fat and is a predisposing risk factor with associated complex metabolic syndromes in the human population. Preclinical rodent models play a pivotal role in understanding the pathogenesis of obesity and development of new treatment strategies for humans. High-fat-diet (HFD)-induced rodents are used for chronic obesity models owing to their quick adaptation to high-fat diets and rapid body weight gain and different rats (Wistar Sprague-Dawley and Lewis) have been used by various researchers. However, the selection of appropriate stock contributes to the translation of clinically linked disease phenotypes to preclinical animal models.MethodsThe study was conducted using two commonly used rat stocks Hsd:Sprague-Dawley (SD) and Crl:Charles River (CD) to develop a chronic high-fat-diet-induced obesity model (DIO) to explore the underlying mechanisms of obesity and its utilization in drug discovery and development during preclinical stages. In addition two high-fat diets of different composition were evaluated (D12327; 40% kcal fat and D12492; 60% kcal fat) for their potential to induce obesity using these two stocks.ResultsA differential sensitivity to HFD was observed in body weight gain fat mass composition and obesity-linked symptoms such as impaired glucose tolerance insulin and leptin levels. The comparative research findings of Hsd:SD and Crl:CD rat stocks suggested that Crl:CD rats are more prone to diet-induced obesity and its associated complications.ConclusionsCrl:CD rats were found to be a suitable model for obesity over Hsd:SD when considering the important hallmarks of metabolic disorders that may be utilized for obesity-related research.

Eisenia bicyclis Inhibits Body Weight Gain and Fat Accumulation Induced by High-Fat Diets in Mice

2010 ◽  
Vol 15 (4) ◽  
pp. 262-266 ◽  
Author(s):  
Won-Hee Choi ◽  
Ji-Yun Ahn ◽  
Sun-A Kim ◽  
Tae-Wan Kim ◽  
Tae-Youl Ha
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Body Weight Gain ◽  
High Fat ◽  
Eisenia Bicyclis ◽  
Fat Accumulation ◽  
High Fat Diets ◽  
Fat Diets

Abstract 75: Chronic Treatment With At2 Receptor Agonist Rescues High Fat Diet-induced Obesity in Female Mice.

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Mohammed A Khan ◽  
Preethi Samuel ◽  
Sourashish Nag ◽  
Tahir Hussain
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
The Body ◽  
Calorie Intake ◽  
Adipocyte Size ◽  
High Fat ◽  
Female Mice ◽  
Diet Induced Obesity

Obesity in itself is a disease condition and a major risk factor in the development of hypertension, dyslipidemia, and hyperglycemia. Therefore, successful strategies for improving obesity and related metabolic risk factors are needed. Role of renin-angiotensin system (RAS) has been implicated in obesity and metabolic dysfunction. Recently, we have shown that AT2R knock-out in female mice caused a greater body weight gain and hyperinsulimia in response to high fat diet (HFD). In the present study, we hypothesize that AT2R activation rescues diet-induced obesity in females. To test this hypothesis, we injected AT2R non-peptide agonist C21 (0.3mg/kg/day i.p) in C57BL6 female mice on HFD for 12 weeks. C21-treatment did not affect the HFD calorie intake (HFD: 937±18 Kcal; C21HFD: 886±37 Kcal) but caused lesser body weight gain compared to control (HFD: 4.4± 0.4g; C21HFD: 3.06± 0.4g). Similar to the body weight gain pattern, gonadal fat weight and adipocyte size were decreased significantly in C21-treated mice on HFD compared to control HFD group (HFD: 4.4± 0.4 g; C21 HFD: 3.06± 0.4g) and (HFD: 6404±161.6μm2 ; C21HFD: 3874±103.2μm2 ) respectively. Moreover, the C21-treated females on HFD had lower levels of plasma insulin, improved glucose tolerance, and decreased plasma free fatty acids and hepatic triglycerides. Western blot revealed that phospho-Ser79-acetyl CoA carboxylase (p-Ser79-ACC-1) was reduced, an index of increased lipogenic activity and decreased β-oxidation process, in both adipose (Adi) and hepatic (Hep) tissues of HFD fed groups (Adi: 86% and Hep: 73% of 100% controls); C21-treatment revered the decrease in p-ser79-ACC-1 in Adi (104% of control) and caused an increase in Hep (122% of control) respectively. The HFD feeding lowered the estradiol level (ND: 38.8±2.6 vs HFD:11.3±1.2ng), which was modestly reversed by C21 treatment (C21HFD:17.4± 1.5ng) in HFD mice. Our results strongly suggest that stimulation of AT2R in female mice positively contribute, predominantly independent of estrogen, to rescue body weight gain and adipocyte size increase in response to HFD. We propose reduced lipogenesis and enhanced lipid β-oxidation as potential mechanisms linked to AT2R action in reducing obesity and its related metabolic disorders in females.

scholarly journals Tetrahydro iso-Alpha Acids from Hops Improve Glucose Homeostasis and Reduce Body Weight Gain and Metabolic Endotoxemia in High-Fat Diet-Fed Mice

PLoS ONE ◽  
2012 ◽  
Vol 7 (3) ◽  
pp. e33858 ◽  
Author(s):  
Amandine Everard ◽  
Lucie Geurts ◽  
Marie Van Roye ◽  
Nathalie M. Delzenne ◽  
Patrice D. Cani
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Glucose Homeostasis ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
High Fat ◽  
Reduce Body Weight ◽  
Metabolic Endotoxemia

scholarly journals High-fat and low-fat (behavioural) phenotypes: biology or environment?

1999 ◽  
Vol 58 (4) ◽  
pp. 773-777 ◽  
Author(s):  
John E. Blundell ◽  
John Cooling
Keyword(s):  
Risk Factors ◽  
Body Weight ◽  
Risk Factor ◽  
Weight Gain ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Positive Energy ◽  
High Fat ◽  
Low Fat ◽  
Conceptual Tool

It is now widely accepted that obesity develops by way of genetic mechanisms conferring specific dispositions which interact with strong environmental pressures. It is also accepted that certain dispositions constitute metabolic risk factors for weight gain. It is less well accepted that certain patterns of behaviour (arising from biological demands or environmental influences) put individuals at risk of developing a positive energy balance and weight gain (behavioural risk factors). Relevant patterns of behaviour include long-lasting habits for selecting and eating particular types of foods. Such habits define two distinct groups characterized as high-fat (HF) and low-fat (LF) phenotypes. These habits are important because of the attention given to dietary macronutrients in body-weight gain and the worldwide epidemic of obesity. Considerable evidence indicates that the total amount of dietary fat consumed remains the most potent food-related risk factor for weight gain. However, although habitual intake of a high-fat diet is a behavioural risk factor for obesity, it does not constitute a biological inevitability. A habitual low-fat diet does seem to protect against the development of obesity, but a high-fat diet does not guarantee that an individual will be obese. Although obesity is much more prevalent among HF than LF, some HF are lean with BMI well within the normal range. The concept of 'different routes to obesity' through a variety of nutritional scenarios can be envisaged, with predisposed individuals varying in their susceptibility to different dietary inputs. In a particular subgroup of individuals (young adult males) HF and LF displayed quite different profiles of appetite control, response to nutrient challenges and physiological measures, including BMR, RQ, heart rate, plasma leptin levels and thermogenic responses to fat and carbohydrate meals. These striking differences suggest that HF and LF can be used as a conceptual tool to investigate the relationship between biology and the environment (diet) in the control of body weight.

scholarly journals Adult offspring of high-fat diet-fed dams can have normal glucose tolerance and body composition

2014 ◽  
Vol 5 (3) ◽  
pp. 229-239 ◽  
Author(s):  
K. M. Platt ◽  
R. J. Charnigo ◽  
K. J. Pearson
Keyword(s):  
Body Composition ◽  
Body Weight ◽  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
High Fat Diet ◽  
High Fat ◽  
High Fat Diets ◽  
Normal Glucose ◽  
Fat Diets

Maternal high-fat diet consumption and obesity have been shown to program long-term obesity and lead to impaired glucose tolerance in offspring. Many rodent studies, however, use non-purified, cereal-based diets as the control for purified high-fat diets. In this study, primiparous ICR mice were fed purified control diet (10–11 kcal% from fat of lard or butter origin) and lard (45 or 60 kcal% fat) or butter (32 or 60 kcal% fat)-based high-fat diets for 4 weeks before mating, throughout pregnancy, and for 2 weeks of nursing. Before mating, female mice fed the 32 and 60% butter-based high-fat diets exhibited impaired glucose tolerance but those females fed the lard-based diets showed normal glucose disposal following a glucose challenge. High-fat diet consumption by female mice of all groups decreased lean to fat mass ratios during the 4th week of diet treatment compared with those mice consuming the 10–11% fat diets. All females were bred to male mice and pregnancy and offspring outcomes were monitored. The body weight of pups born to 45% lard-fed dams was significantly increased before weaning, but only female offspring born to 32% butter-fed dams exhibited long-term body weight increases. Offspring glucose tolerance and body composition were measured for at least 1 year. Minimal, if any, differences were observed in the offspring parameters. These results suggest that many variables should be considered when designing future high-fat diet feeding and maternal obesity studies in mice.

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